Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.Autoimmune Diseases: Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Autoantigens: Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.Diabetes Mellitus, Type 1: A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.Mercuric Chloride: Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.Lupus Erythematosus, Systemic: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.Antibodies, Antinuclear: Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.Self Tolerance: The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.T-Lymphocytes, Regulatory: CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.Mice, Inbred C57BLImmune Tolerance: The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.Thyroiditis, Autoimmune: Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.Mice, Inbred NOD: A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.Lymphocyte Activation: Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.B-Lymphocytes: Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.Mice, Inbred MRL lpr: A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.Mice, Inbred NZBMice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Encephalomyelitis, Autoimmune, Experimental: An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)Autoimmune Diseases of the Nervous System: Disorders caused by cellular or humoral immune responses primarily directed towards nervous system autoantigens. The immune response may be directed towards specific tissue components (e.g., myelin) and may be limited to the central nervous system (e.g., MULTIPLE SCLEROSIS) or the peripheral nervous system (e.g., GUILLAIN-BARRE SYNDROME).Glutamate Decarboxylase: A pyridoxal-phosphate protein that catalyzes the alpha-decarboxylation of L-glutamic acid to form gamma-aminobutyric acid and carbon dioxide. The enzyme is found in bacteria and in invertebrate and vertebrate nervous systems. It is the rate-limiting enzyme in determining GAMMA-AMINOBUTYRIC ACID levels in normal nervous tissues. The brain enzyme also acts on L-cysteate, L-cysteine sulfinate, and L-aspartate. EC 4.1.1.15.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.CD4-Positive T-Lymphocytes: A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).Interleukin-17: A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.Islets of Langerhans: Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Models, Immunological: Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.Forkhead Transcription Factors: A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.T-Lymphocyte Subsets: A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.Dendritic Cells: Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).Mice, Inbred BALB CPolyendocrinopathies, Autoimmune: Autoimmune diseases affecting multiple endocrine organs. Type I is characterized by childhood onset and chronic mucocutaneous candidiasis (CANDIDIASIS, CHRONIC MUCOCUTANEOUS), while type II exhibits any combination of adrenal insufficiency (ADDISON'S DISEASE), lymphocytic thyroiditis (THYROIDITIS, AUTOIMMUNE;), HYPOPARATHYROIDISM; and gonadal failure. In both types organ-specific ANTIBODIES against a variety of ENDOCRINE GLANDS have been detected. The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Spleen: An encapsulated lymphatic organ through which venous blood filters.Insulin Antibodies: Antibodies specific to INSULIN.Thyroid Gland: A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.Th17 Cells: Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.Lupus Vulgaris: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.B-Cell Activating Factor: A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN.Thymus Gland: A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.Protein Tyrosine Phosphatase, Non-Receptor Type 22: A subtype of non-receptor protein tyrosine phosphatases that is characterized by the presence of an N-terminal catalytic domain and a C-terminal PROLINE-rich domain. The phosphatase subtype is predominantly expressed in LYMPHOCYTES and plays a key role in the inhibition of downstream T-LYMPHOCYTE activation. Polymorphisms in the gene that encodes this phosphatase subtype are associated with a variety of AUTOIMMUNE DISEASES.T-Lymphocytes, Helper-Inducer: Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.Hashimoto Disease: Chronic autoimmune thyroiditis, characterized by the presence of high serum thyroid AUTOANTIBODIES; GOITER; and HYPOTHYROIDISM.Receptors, Antigen, T-Cell: Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.Molecular Mimicry: The structure of one molecule that imitates or simulates the structure of a different molecule.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.ThyroglobulinB-Lymphocyte Subsets: A classification of B-lymphocytes based on structurally or functionally different populations of cells.CTLA-4 Antigen: An inhibitory T CELL receptor that is closely related to CD28 ANTIGEN. It has specificity for CD80 ANTIGEN and CD86 ANTIGEN and acts as a negative regulator of peripheral T cell function. CTLA-4 antigen is believed to play role in inducing PERIPHERAL TOLERANCE.Iodide Peroxidase: A hemeprotein that catalyzes the oxidation of the iodide radical to iodine with the subsequent iodination of many organic compounds, particularly proteins. EC 1.11.1.8.Lymphopenia: Reduction in the number of lymphocytes.Multiple Sclerosis: An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)Thyroid Diseases: Pathological processes involving the THYROID GLAND.HLA-DQ Antigens: A group of the D-related HLA antigens found to differ from the DR antigens in genetic locus and therefore inheritance. These antigens are polymorphic glycoproteins comprising alpha and beta chains and are found on lymphoid and other cells, often associated with certain diseases.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Th1 Cells: Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.Interferon-gamma: The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.B-Lymphocytes, Regulatory: B-cells that have a role in regulating the immune response including the production of CYTOKINES. This function is in addition to their traditional role in making antibodies.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Mice, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.HLA-DQ beta-Chains: Transmembrane proteins that form the beta subunits of the HLA-DQ antigens.CD8-Positive T-Lymphocytes: A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.Splenomegaly: Enlargement of the spleen.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Collagen Type V: A fibrillar collagen found widely distributed as a minor component in tissues that contain COLLAGEN TYPE I and COLLAGEN TYPE III. It is a heterotrimeric molecule composed of alpha1(V), alpha2(V) and alpha3(V) subunits. Several forms of collagen type V exist depending upon the composition of the subunits that form the trimer.Antigens, CD: Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.Graves Disease: A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).Peripheral Tolerance: The mechanism, in peripheral lymphoid organs (LYMPH NODES; SPLEEN; TONSILS; and mucosal-associated lymphoid tissue), that prevents mature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished through a variety of means including CLONAL ANERGY and CLONAL DELETION.Antigen Presentation: The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)Immunity, Innate: The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Mice, Congenic: Mouse strains constructed to possess identical genotypes except for a difference at a single gene locus.Lupus Nephritis: Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Arthritis, Rheumatoid: A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.Mice, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Myelin-Oligodendrocyte Glycoprotein: A transmembrane protein present in the MYELIN SHEATH of the CENTRAL NERVOUS SYSTEM. It is one of the main autoantigens implicated in the pathogenesis of MULTIPLE SCLEROSIS.Interleukin-2 Receptor alpha Subunit: A low affinity interleukin-2 receptor subunit that combines with the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN to form a high affinity receptor for INTERLEUKIN-2.Sjogren's Syndrome: Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.Hypergammaglobulinemia: An excess of GAMMA-GLOBULINS in the serum due to chronic infections or PARAPROTEINEMIAS.Histocompatibility Antigens Class II: Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection.Receptor-Like Protein Tyrosine Phosphatases, Class 8: A subclass of receptor-like protein tryosine phosphatases that contain an extracellular RDGS-adhesion recognition motif and a single cytosolic protein tyrosine phosphate domain.Myelin Basic Protein: An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.Immunomodulation: Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include IMMUNIZATION or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.Immune System: The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.Uveitis: Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)Immunization: Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Antibody Formation: The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.Thymectomy: Surgical removal of the thymus gland. (Dorland, 28th ed)Thyroiditis: Inflammatory diseases of the THYROID GLAND. Thyroiditis can be classified into acute (THYROIDITIS, SUPPURATIVE), subacute (granulomatous and lymphocytic), chronic fibrous (Riedel's), chronic lymphocytic (HASHIMOTO DISEASE), transient (POSTPARTUM THYROIDITIS), and other AUTOIMMUNE THYROIDITIS subtypes.Antigen-Presenting Cells: A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.Stiff-Person Syndrome: A condition characterized by persistent spasms (SPASM) involving multiple muscles, primarily in the lower limbs and trunk. The illness tends to occur in the fourth to sixth decade of life, presenting with intermittent spasms that become continuous. Minor sensory stimuli, such as noise and light touch, precipitate severe spasms. Spasms do not occur during sleep and only rarely involve cranial muscles. Respiration may become impaired in advanced cases. (Adams et al., Principles of Neurology, 6th ed, p1492; Neurology 1998 Jul;51(1):85-93)Mice, Inbred DBAArthritis, Experimental: ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.Epitopes: Sites on an antigen that interact with specific antibodies.Th2 Cells: Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.Infection: Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.Adaptive Immunity: Protection from an infectious disease agent that is mediated by B- and T- LYMPHOCYTES following exposure to specific antigen, and characterized by IMMUNOLOGIC MEMORY. It can result from either previous infection with that agent or vaccination (IMMUNITY, ACTIVE), or transfer of antibody or lymphocytes from an immune donor (IMMUNIZATION, PASSIVE).Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Rats, Inbred LewRats, Inbred BB: A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).Immunoglobulin M: A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified.Lymphatic Diseases: Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.Receptors, Interleukin-2: Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Interleukin-10: A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.Immunologic Deficiency Syndromes: Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral.Antigens: Substances that are recognized by the immune system and induce an immune reaction.Clonal Anergy: Functional inactivation of T- or B-lymphocytes rendering them incapable of eliciting an immune response to antigen. This occurs through different mechanisms in the two kinds of lymphocytes and can contribute to SELF TOLERANCE.Interleukin-2: A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Interleukin-23: A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-23 is comprised of a unique 19 kDa subunit and 40 kDa subunit that is shared with INTERLEUKIN-12. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cellsLymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation.HLA-DR Antigens: A subclass of HLA-D antigens that consist of alpha and beta chains. The inheritance of HLA-DR antigens differs from that of the HLA-DQ ANTIGENS and HLA-DP ANTIGENS.Antigens, Differentiation: Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.Islets of Langerhans Transplantation: The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.Crosses, Genetic: Deliberate breeding of two different individuals that results in offspring that carry part of the genetic material of each parent. The parent organisms must be genetically compatible and may be from different varieties or closely related species.ArthritisAllergy and Immunology: A medical specialty concerned with the hypersensitivity of the individual to foreign substances and protection from the resultant infection or disorder.Clonal Deletion: Removal, via CELL DEATH, of immature lymphocytes that interact with antigens during maturation. For T-lymphocytes this occurs in the thymus and ensures that mature T-lymphocytes are self tolerant. B-lymphocytes may also undergo clonal deletion.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.Immunity, Cellular: Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.Receptors, Antigen, B-Cell: IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.Myocarditis: Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.Epitopes, T-Lymphocyte: Antigenic determinants recognized and bound by the T-cell receptor. Epitopes recognized by the T-cell receptor are often located in the inner, unexposed side of the antigen, and become accessible to the T-cell receptors after proteolytic processing of the antigen.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Anemia, Hemolytic, Autoimmune: Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.Lymphocyte Count: The number of LYMPHOCYTES per unit volume of BLOOD.Receptors, Antigen, T-Cell, alpha-beta: T-cell receptors composed of CD3-associated alpha and beta polypeptide chains and expressed primarily in CD4+ or CD8+ T-cells. Unlike immunoglobulins, the alpha-beta T-cell receptors recognize antigens only when presented in association with major histocompatibility (MHC) molecules.Immunoglobulins: Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Insulin-Secreting Cells: A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable.Glomerulonephritis: Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.Lymph Nodes: They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.B-Cell Activation Factor Receptor: A member of the tumor necrosis factor receptor superfamily that specifically binds B-CELL ACTIVATING FACTOR. It is found on B-LYMPHOCYTES and plays a role in maturation and survival of B-cells. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Antigens, CD4: 55-kDa antigens found on HELPER-INDUCER T-LYMPHOCYTES and on a variety of other immune cell types. CD4 antigens are members of the immunoglobulin supergene family and are implicated as associative recognition elements in MAJOR HISTOCOMPATIBILITY COMPLEX class II-restricted immune responses. On T-lymphocytes they define the helper/inducer subset. CD4 antigens also serve as INTERLEUKIN-15 receptors and bind to the HIV receptors, binding directly to the HIV ENVELOPE PROTEIN GP120.Immunity, Humoral: Antibody-mediated immune response. Humoral immunity is brought about by ANTIBODY FORMATION, resulting from TH2 CELLS activating B-LYMPHOCYTES, followed by COMPLEMENT ACTIVATION.Alopecia Areata: Loss of scalp and body hair involving microscopically inflammatory patchy areas.Antigens, CD95: A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.Rats, Inbred BNAntibody Specificity: The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.Germinal Center: The activated center of a lymphoid follicle in secondary lymphoid tissue where B-LYMPHOCYTES are stimulated by antigens and helper T cells (T-LYMPHOCYTES, HELPER-INDUCER) are stimulated to generate memory cells.Antigens, CD80: A costimulatory ligand expressed by ANTIGEN-PRESENTING CELLS that binds to CTLA-4 ANTIGEN with high specificity and to CD28 ANTIGEN with low specificity. The interaction of CD80 with CD28 ANTIGEN provides a costimulatory signal to T-LYMPHOCYTES, while its interaction with CTLA-4 ANTIGEN may play a role in inducing PERIPHERAL TOLERANCE.Immunologic Memory: The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.Pemphigus: Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.Demyelinating Autoimmune Diseases, CNS: Conditions characterized by loss or dysfunction of myelin (see MYELIN SHEATH) in the brain, spinal cord, or optic nerves secondary to autoimmune mediated processes. This may take the form of a humoral or cellular immune response directed toward myelin or OLIGODENDROGLIA associated autoantigens.Immunophenotyping: Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.Virus Diseases: A general term for diseases produced by viruses.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Rheumatoid Factor: Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.Scleroderma, Systemic: A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.CD40 Ligand: A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. Mutation of the gene for CD40 ligand is a cause of HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 1.Transplantation Tolerance: An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.Interleukin-4: A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. (1/3192)

The fine specificity of the Ro and La proteins has been studied by several techniques. In general, there is agreement in a qualitative sense that autoantibodies bind multiple epitopes. For some specific antibody binding, different studies agree quantitatively, for instance, the binding of the carboxyl terminus of 60-kd Ro as described by 2 studies using different techniques and the presence of an epitope within the leucine zipper of 52-kd Ro. In addition, there is general agreement about the location of a prominent epitope at the RRM motif region of the La molecule. On the other hand, the many specific epitope regions of the molecules differ among these studies. These discrepancies are likely the result of using different techniques, sera, and peptide constructs as well as a result of inherent advantages and disadvantages in the individual approaches. Several theories concerning the origin of not only the antibodies, but also the diseases themselves, have been generated from studies of the fine specificity of antibody binding. These include a theory of a primordial foreign antigen for anti-Ro autoimmunity, molecular mimicry with regard to La and CCHB, as well as the association of anti-Ro with HLA. These remain unproven, but are of continuing interest. An explanation for the association of anti-60-kd Ro and anti-52-kd Ro in the sera of patients has sprung from evaluating antibody binding. Data demonstrating multiple epitopes are part of a large body of evidence that strongly suggests an antigen-driven immune response. This means that the autoantigens are directly implicated in initiating and sustaining autoimmunity in their associated diseases. A number of studies have investigated the possibility of differences in the immune response to these antigens in SS and SLE sera. While several differences have been reported, none have been reproduced in a second cohort of patients. Furthermore, none of the reported differences may be sufficiently robust for clinical purposes, such as distinguishing between SS with systemic features and mild SLE, although some might be promising. For instance, in at least 3 groups of SLE patients, no binding of residues spanning amino acids 21-41 of 60-kd Ro has been found. Meanwhile, 1 of those studies found that 41% of sera from patients with primary SS bound the 60-kd Ro peptide 21-41. Perhaps future studies will elaborate a clinical role of such a difference among SS and SLE patients. Study of the epitopes of these autoantigens has, in part, led to a new animal model of anti-Ro and anti-La. Non-autoimmune-prone animals are immunized with proteins or peptides that make up the Ro/La RNP. Such animals develop an autoimmune response to the entire particle, not just the immunogen. This response has been hypothesized to arise from autoreactive B cells. In another, older animal model of disease, the MRL-lpr/lpr mouse, B cells have recently been shown to be required for the generation of abnormal, autoreactive T cells. Thus, there are now powerful data indicating that B cells that produce autoantibodies are directly involved in the pathogenesis of disease above and beyond the formation of immune complexes. Given that the autoreactive B cell is potentially critical to the underlying pathogenesis of disease, then studying these cells will be crucial to further understanding the origin of diseases associated with Ro and La autoimmunity. Hopefully, an increased understanding will eventually lead to improved treatment of patients. Progress in the area of treatment will almost surely be incremental, and studies of the fine specificity of autoantibody binding will be a part of the body of basic knowledge contributing to ultimate advancement. In the future, the animal models will need to be examined with regard to immunology and immunochemistry as well as genetics. The development of these autoantibodies has not been studied extensively because upon presentation to medical care, virtually all patients have a full-  (+info)

Development and function of autospecific dual TCR+ T lymphocytes. (2/3192)

Recent studies have challenged the long held concept that each T lymphocyte expresses on its surface only a single, unique alphabetaTCR. Dual TCR+ T cells have been recognized, however, their origin and potential to escape screening for self-reactivity remain obscure. We now report the thymic generation of dual alphabetaTCR+ T cells in the H-2Db/H-Y-specific TCR transgenic (Tg) mouse. Dual TCR+ thymocytes were positively selected less efficiently than single TCR+ thymocytes, although a subset attained maturity. Importantly, when TCR Tg mice were bred onto a negatively selecting background, auto-specific cells survived central deletion and matured as CD4+ dual TCR+ cells. These cells were autoreactive when CD8 expression was restored. The existence of autospecific, dual TCR+ T cells may have implications for the maintenance of self tolerance.  (+info)

Induction of autoimmunity by multivalent immunodominant and subdominant T cell determinants of La (SS-B). (3/3192)

We investigated the consequences of altering the form and valence of defined autodeterminants on the initiation and spreading of experimentally induced La/Ro autoimmunity. Anti-La and Ro (SS-A) Ab responses were monitored following immunization of healthy mice with defined immunodominant and subdominant T cell determinants of the La (SS-B) autoantigen synthesized as either monomeric or multiple antigenic (MAP) peptides. Abs to mouse La (mLa) developed faster and were of higher titer in mice immunized with the subdominant mLa25-44 MAP compared with mice immunized with the 25-44 monomer. Rapid intermolecular spreading of the autoimmune response to 60-kDa Ro was observed in AKR/J mice immunized with mLa25-44 MAP, but not in mice immunized repeatedly with monomeric peptide. A/J mice immunized and boosted with the known tolerogenic mLa287-301 determinant delivered as monomeric peptide failed to develop Abs to either intact mLa or mLa287-301 peptide. However, immunization with the multivalent mLa287-301 peptide led to the rapid production of high titer mLa autoantibodies associated with a proliferative T cell response to the mLa287-301 peptide. The data suggested that the enhanced immunogenicity of MAPs was not due to augmented Ag presentation or T cell stimulation. However, MAP-, but not monomer peptide-, containing immune complexes were potent substrates for Ab-dependent fixation of complement. These results demonstrate that the form of Ag responsible for inducing autoimmunity can profoundly influence the nature and magnitude of the immune response. Thus, molecular mimicry of tolerogenic and nontolerogenic self determinants might trigger autoimmunity under conditions of altered valence.  (+info)

Clinical, biochemical and molecular genetic features of Leber's hereditary optic neuropathy. (4/3192)

Leber's hereditary optic neuropathy (LHON) has traditionally been considered a disease causing severe and permanent visual loss in young adult males. In nearly all families with LHON it is associated with one of three pathogenic mitochondrial DNA (mtDNA) mutations, at bp 11778, 3460 or 14484. The availability of mtDNA confirmation of a diagnosis of LHON has demonstrated that LHON occurs with a wider range of age at onset and more commonly in females than previously recognised. In addition, analysis of patients grouped according to mtDNA mutation has demonstrated differences both in the clinical features of visual failure and in recurrence risks to relatives associated with each of the pathogenic mtDNA mutations. Whilst pathogenic mtDNA mutations are required for the development of LHON, other factors must be reponsible for the variable penetrance and male predominance of this condition. Available data on a number of hypotheses including the role of an additional X-linked visual loss susceptibility locus, impaired mitochondrial respiratory chain activity, mtDNA heteroplasmy, environmental factors and autoimmunity are discussed. Subacute visual failure is seen in association with all three pathogenic LHON mutations. However, the clinical and experimental data reviewed suggest differences in the phenotype associated with each of the three mutations which may reflect variation in the disease mechanisms resulting in this common end-point.  (+info)

Vaccination with a recombinant vaccinia virus encoding a "self" antigen induces autoimmune vitiligo and tumor cell destruction in mice: requirement for CD4(+) T lymphocytes. (5/3192)

Many human and mouse tumor antigens are normal, nonmutated tissue differentiation antigens. Consequently, immunization with these "self" antigens could induce autoimmunity. When we tried to induce immune responses to five mouse melanocyte differentiation antigens, gp100, MART-1, tyrosinase, and tyrosinase-related proteins (TRP) 1 and TRP-2, we observed striking depigmentation and melanocyte destruction only in the skin of mice inoculated with a vaccinia virus encoding mouse TRP-1. These mice rejected a lethal challenge of B16 melanoma, indicating the immune response against TRP-1 could destroy both normal and malignant melanocytes. Cytotoxic T lymphocytes specific for TRP-1 could not be detected in depigmented mice, but high titers of IgG anti-TRP-1 antibodies were present. Experiments with knockout mice revealed an absolute dependence on major histocompatibility complex class II, but not major histocompatibility complex class I, for the induction of both vitiligo and tumor protection. Together, these results suggest that the deliberate induction of self-reactivity using a recombinant viral vector can lead to tumor destruction, and that in this model, CD4(+) T lymphocytes are an integral part of this process. Vaccine strategies targeting tissue differentiation antigens may be valuable in cancers arising from nonessential cells and organs such as melanocytes, prostate, testis, breast, and ovary.  (+info)

Autoimmunity resulting from cytokine treatment predicts long-term survival in patients with metastatic renal cell cancer. (6/3192)

PURPOSE: In patients undergoing cytokine therapy, systemically applied interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha) have been reported to induce thyroid dysfunction as well as thyroid autoantibodies. We analyzed the correlation of thyroid autoimmunity with HLA phenotype, various other autoimmune parameters, and patient survival. PATIENTS AND METHODS: For this purpose, antithyroglobulin autoantibodies, antimicrosomal thyroid autoantibodies, thyroglobulin receptor autoantibodies, thyroid dysfunction, and multiple clinical parameters were determined in 329 unselected patients with metastatic renal cell cancer before and after systemic IL-2 and IFN-alpha2 therapy. For statistical analysis, we used both univariate and multivariate Cox proportional hazards models and the two-tailed Fisher's exact test. RESULTS: Antithyroglobulin autoantibodies and antimicrosomal thyroid autoantibodies were detected in 60 patients (18%); positive autoantibody titers of various other autoimmune parameters were statistically unrelated. The presence of thyroid autoantibodies was correlated with prolonged survival (P<.0001). There was a statistically significant difference in frequencies of HLA-Cw7 expression between thyroid autoantibody-positive and -negative patients (P< or =.05), and the Cw7 expression was associated with prolonged overall survival (P = .009). CONCLUSION: The evaluation of thyroid autoantibodies during cytokine therapy could be a useful prognostic marker for patients with renal cell carcinoma who benefit from cytokine treatment. IL-2- and IFN-alpha2-induced tumor control and prolonged survival may require breaking of immunologic tolerance against self-antigens.  (+info)

Evidence of cell-mediated cardiac myocyte injury involved in the heart failure of a patient with progressive systemic sclerosis. (7/3192)

A 54-year-old woman with progressive systemic sclerosis (PSS) was admitted to hospital because of dyspnea and chest pain. Echocardiogram revealed diffuse hypokinesis of the left ventricle (ejection fraction 24%). Methylprednisolone, heparin, and diuretics were administered, without benefit. Anemia, thrombocytopenia, and renal dysfunction rapidly progressed, and she died of heart failure on the 14th hospital day. Immunohistochemical study of the myocardial tissue showed mild to moderate cell infiltration, mainly consisting of natural killer (NK) cells, macrophages, cytotoxic T lymphocytes (CTLs), and T helper cells. Perforin, a cytolytic factor, was expressed in the infiltrating CTLs and NK cells, indicating that these cells were activated killer cells. Furthermore, human leukocyte antigen classes I and II, intercellular adhesion molecule-1, as well as costimulatory molecules B7-1, B7-2, and CD40, all of which are known not to be expressed in cardiac myocytes under normal conditions, were moderately to strongly expressed in cardiac myocytes. There was no detectable level of enterovirus genomes in the polymerase chain reaction products from the myocardial tissue of this patient. These findings strongly suggest that the infiltrating killer cells recognized cardiac myocytes as target cells and directly damaged them by releasing perforin. Enhanced expression of these antigens may have played an important role in the activation and cytotoxicity of the infiltrating killer cells. Absence of enterovirus genomes in the myocardial tissue may suggest that this autoimmune process is primarily induced by PSS.  (+info)

Clinical presentation and early course of type 1 diabetes in patients with and without thyroid autoimmunity. (8/3192)

OBJECTIVE: To evaluate the prevalence of thyroid autoimmunity (TAI) in patients with recent-onset type 1 diabetes and to determine the influence of TAI on the clinical presentation and evolution of type 1 diabetes. RESEARCH DESIGN AND METHODS: We studied 111 newly diagnosed type 1 diabetes patients > 13 years old. The diagnosis of TAI was based on medical history and measurement of thyroid peroxidase (microsomal) antibodies (TPOAs). Clinical presentation of diabetes, beta-cell autoimmune markers (GADAs and 1A2As), and evolution of insulin-secretory reserves and metabolic control during the first 2 years of follow-up were analyzed. Differences between groups were evaluated by Student's t test or the chi 2 test. The influence of TAI on follow-up data was evaluated by multiple logistic regression analysis. RESULTS: TAI was present in 31 patients (14 TPOA+ patients with normal thyroid function, 12 TPOA+ patients with thyroid dysfunction, and 5 patients with previously diagnosed TAI). TAI was more prevalent in women than in men (43.7 vs. 15.9%, P = 0.001). beta-Cell autoimmunity was more prevalent in patients with TAI than in those without TAI (93.5 vs. 76.3%, P = 0.03). The evolution of insulin requirements, metabolic control, and insulin-secretory reserves was comparable in the two groups. CONCLUSIONS: TAI is present in many type 1 diabetes patients at the time of diagnosis and is associated with a high prevalence of thyroid dysfunction. The clinical presentation of diabetes and the evolution of metabolic control and insulin-secretory reserves are not influenced by the presence of TAI. Patients with type 1 diabetes should be screened for TAI at diagnosis.  (+info)

TY - JOUR. T1 - Definition of human autoimmunity - autoantibodies versus autoimmune disease. AU - Lleo, Ana. AU - Invernizzi, Pietro. AU - Gao, Bin. AU - Podda, Mauro. AU - Gershwin, M. Eric. PY - 2010/3. Y1 - 2010/3. N2 - The critical function of the immune system is to discriminate self from non-self. Tolerance against self-antigens is a highly regulated process and, in order to maintain it, the immune system must be able to distinguish self-reactive lymphocytes as they develop. The presence of autoantibodies is the consequence of breakdown of tolerance and, although they are an important serological feature of autoimmune diseases, their presence is not exclusive of these conditions. Antibodies against self-antigens are also found in cancer, during massive tissue damage and even in healthy subjects. Natural autoantibodies provide immediate protection against infection and also prevent inflammation by facilitating the clearance of oxidized lipids, oxidized proteins, and apoptotic cells; their ...
Although high expression of most B7 family members is largely restricted to immune cells, especially APCs, we were not able to detect protein expression of B7x in any cell type of hematopoietic origin. This strongly suggested that B7x does not play a role in regulating T cell priming in the lymphoid organs. However, histological staining of pancreatic sections demonstrated constitutive expression of B7x in the islets of Langerhans, indicating that this inhibitory molecule may have a role in maintaining peripheral tolerance to islet-reactive T cells. It has already been shown that PD-L1, another member of the B7 family, plays an important role in preventing diabetes by inhibiting islet-reactive T cells (Ansari et al., 2003). Although PD-L1 has been reported to be expressed at very low levels (Liang et al., 2003) or absent (Ansari et al., 2003) in naive pancreata, its expression is up-regulated in an age-dependent manner in NOD mice. Using bone marrow chimeras, it was shown that PD-L1 expression ...
Understanding the mode of action of genes influencing the development of type 1 diabetes requires knowledge as to whether genes influence the development of islet autoimmunity and/or progression from autoimmunity to diabetes. Here we have examined association in a cohort of genetically at-risk children who were followed from birth for both development of islet autoantibodies and diabetes. An association of the IFIH1 gene with diabetes development in this cohort allowed us to determine at what stage the gene is likely to influence diabetes development. Unlike HLA class II genes, which strongly influence the risk for developing islet autoantibodies (5-7), association of the IFIH1 gene was restricted to the progression to diabetes after development of islet autoimmunity. In view of the involvement of the IFIH1 gene in responses to virus infection (16,17), the findings are consistent with a role of infection in determining the progression to diabetes after islet autoimmunity has been ...
A better understanding of the molecules involved in immune responses has identified many potential targets for the treatment of autoimmune diseases. But although successful therapies have been found for immune disorders in animal studies, few have passed the much harder test of treating human diseases. So far, non-antigen-specific approaches, such as the blocking of tumour-necrosis factor, are achieving some success but the same is not true for antigen-specific approaches. Future therapies will probably include both non-antigen-specific strategies that target cytokines (cell-cell signalling molecules) or block the molecules that stimulate immune responses, and antigen-specific therapies that induce tolerance to self antigens.
TY - JOUR. T1 - Increased serum IgM, immunodeficiency, and autoimmunity. T2 - A clinical series. AU - Picchianti Diamanti, Andrea. AU - Rosado, M. Manuela. AU - Scarsella, Marco. AU - Ceccarelli, Sara. AU - Laganà, Bruno. AU - DAmelio, Raffaele. AU - Carsetti, Rita. PY - 2015/12/1. Y1 - 2015/12/1. N2 - Background: Primary immunodeficiencies (PIDs) are generally characterized by recurrent infections; however they may be complicated by other clinical disorders such as allergy, autoimmunity, and lymphoproliferation. In particular, autoimmunity may be the first manifestation of the disease in patients with low serum immunoglobulins (Ig) levels. Here we describe a group of patients that share features of immunodeficiency and autoimmunity. Materials and Methods: All patients went through a complete T and B cell subset characterization and a B cell function analysis in the peripheral blood by flow-cytometry. B cell proliferation and plasma cell differentiation was measured, in vitro, after CpG ...
Systemic autoimmunity is thought to result from a mix of genetics, environmental factors and stochastic events [6]. Given the multitude of susceptibility genes, symptoms and immunological abnormalities, it is clear that numerous pathogenic pathways contribute to systemic autoimmune disease [5, 11, 12]. A major thrust of systemic autoimmunity research has centered on elucidation of abnormalities in the adaptive immune response [13, 14]. However more recent research has identified the innate immune response as a major player in the initiation and expansion of systemic autoimmune pathology [4, 5, 9, 15, 16].. The current paradigm for the disease process of idiopathic systemic lupus-like autoimmunity argues for a central role of type I IFN [15, 17, 18]. This is based on the early observation of increased expression of IFN-α inducible genes (or IFN signature) in the peripheral blood cells of patients with SLE [17]. The type I IFN signature is found in 60% to 70% of patients with SLE, ...
Curing type 1 diabetes by islet transplantation requires overcoming both allorejection and recurrent autoimmunity. This has been achieved with systemic immunosuppression, but tolerance induction would be preferable. Most islet allotransplant tolerance induction protocols have been tested in nonobese diabetic (NOD) mice, and most have failed. Failure has been attributed to the underlying autoimmunity, assuming that autoimmunity and resistance to transplantation tolerance have a common basis. Out of concern that NOD biology could be misleading in this regard, we tested the hypothesis that autoimmunity and resistance to transplantation tolerance in NOD mice are distinct phenotypes. Unexpectedly, we observed that (NOD x C57BL/6)F(1) mice, which have no diabetes, nonetheless resist prolongation of skin allografts by costimulation blockade. Further analyses revealed that the F(1) mice shared the dendritic cell maturation defects and abnormal CD4(+) T cell responses of the NOD but had lost its defects in
Highlights: - Antibiotics being explored for the treatment of cystic fibrosis and muscular dystrophy have the potential to trigger autoimmune disease - . He identified 17 peptides that hadnt been characterized before in cells treated with gentamicin and showed that the peptides were presentable to the immune system. - So even as gentamicin fights the…
Lindop, R., et al. Long-term Ro60 humoral autoimmunity in primary Sjögrens syndrome is maintained by rapid clonal turnover. Clinical Immunology. 0, 148(1). 01/07/2013.. ...
Some people seem to be under the belief that autoimmune conditions such as type-1 diabetes develop as a result of "bad genes". This idea has little evolutionary support…. Theres no doubt that genetics do play a role in the etiology of autoimmunity; however, in most cases, its unlikely to be the primary factor involved. This statement is supported by the fact that the prevalence of autoimmune disease has increased markedly over the past centuries, despite the fact that our genes have changed very little over the same time period. Moreover, its supported by the finding that autoimmune diseases are very rare among hunter-gatherers and other traditional groups of people who live in environments that bear resemblance to the Paleolithic environments in which more than 99% of the evolutionary history of our genus Homo took place (1, 2, 3).. When we think about it, it isnt surprising that foragers rarely develop autoimmunity, given that a persons ability to survive and reproduce in a natural ...
They found that ANA (biomarker for autoimmunity) prevalence for 1988-1991 was 11.0%, while for 1999-2004 it was 11.5%, and for 2011-2012 it was 15.9%. These percentages corresponded to 22, 27, and 41 million affected individuals, respectively. ...
Recent evidences suggest that human gut microbiota with major component as bacteria can induce immunity. It is also known that gut lining depletes with ageing and that there is increased risk of autoimmune and inflammatory disorders with ageing. It is therefore likely that both may be correlated as depletion of gut lining exposes the gut bacterial antigens to host immune mechanisms, which may induce immunity to certain bacterial proteins, but at the same time such immunity may also be auto-immunogenic to host. This autoimmunity may make a protein molecule nonfunctional and thereby may be involved in late onset metabolic, autoimmune and inflammatory disorders such as, Diabetes, Rheumatoid Arthritis, Hyperlipidemias and Cancer. In this in-silico study we found a large number of peptides identical between human and gut bacteria which were binding to HLA-II alleles, and hence, likely to be auto-immunogenic. Further we observed that such autoimmune candidates were enriched in bacterial species belonging to
The best evidence to date shows a significant association between thyroid autoimmunity and depression & anxiety. But what does this mean and what should you do?
Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Autoimmunity Highlights acts as the bridge between the clinic, the laboratory and specialists involved in the complex world of autoimmunity diagnosis, ...
... will publish up-to-date, structured reviews on diverse topics in autoimmunity, written by first-class experts in the field. The...
Autoimmune diseases occur when the immune system attacks and destroys the organs and tissues of its own host. Autoimmunity is the third most common type of disease in the United States. Because there is no cure for autoimmunity, it is extremely important to study the mechanisms that trigger these diseases. Most autoimmune diseases predominantly affect females, indicating a strong sex bias. Various factors, including sex hormones, the presence or absence of a second X chromosome, and sex-specific gut microbiota can influence gene expression in a sex-specific way. These changes in gene expression may, in turn, lead to susceptibility or protection from autoimmunity, creating a sex bias for autoimmune diseases. In this Review we discuss recent findings in the field of sex-dependent regulation of gene expression and autoimmunity.. ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Dear Immunonetters, I would like to bring another player into the Self/non-self discrimination arena. That Being the effect of Anergic T-cells on other autoreactive T-cells.This concept has been discussed in the papers by Lasalle and Hafler ( FASEB J. 8:601-608 1994) and Lombardi et al ( science 264:1587 1994). I agree with the authors that the Anergic T-cells play an important rolein self/nonself discrimination. In summary this is whats happening. The Thymus, site of clonal deletion, is very efficient in removing autoreactive T-cells. But nothing is perfect and some autoreactive cells escape this screening. These T-cells can be safely present in the periphery if the antigens they are reactive to are hidden away from them or not presented to them. This is called Clonal Ignorance. If MHC/AG is presented to the autoreactive T-cell but is not followed by costimulation, the result is Clonal anergy. In these cases the T-cells can recognize the self antigen however the extent of the response stops ...
T cell responses are essential for protection against pathogens but can also be detrimental to the host. Therefore many overlapping mechanisms exist to prevent both the development of autoimmunity and excessive tissue damage during chronic infections. T cell differentiation and effector function are shaped by the integration of different signals from the environment. These signals are orchestrated through a variety of signaling receptors including the T cell receptor, activating (co-stimulatory molecules or cytokines) and inhibitory (checkpoint) receptors. Thus, the modulation of external signals could impact on the development or function of effector and/or regulatory T (Treg) cells. In pre-clinical human or animal studies, the manipulation of T cell function has been attempted via numerous different approaches. These include (i) immune checkpoint blockade (PD-1, PD-L1, Tim3 and/or CTLA-4 among others), (ii) alterations in metabolic pathways and (iii) the utilization of biological agents such as
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We offer a large selection of autoimmunity ELISA kits, it is vital that accurate and reliable assay methods are available to analyse autoimmune diseases for
Major Medline report on latest on causes and details of diabetes type 1 and type 2. Covers latest research on environmental causes of diabetes - details of autoimmunity process - and latest successes in reversing diabetes.
NK cells in CNS inflammation and autoimmunity Project Summary: Natural killer (NK) cells are large, granular lymphocytes that operate through cytolytic activity...
Current Research: My main interest is mechanistic dissection of natural and induced causes that precipitate the pathological state of the immune system, called autoimmunity. Autoimmunity generally clinically manifests as a variety of organ-specific diseases such as Type 1 Diabetes (T1D), for which we have a plethora of mouse models. Progression of T1D involves the activation of autoimmune T cells, consequent honing of activated lymphocytes to the pancreatic islets, and ensuing destruction of insulin-producing beta cells. Our studies focus on determining how autoimmune T cells are initially activated during T1D pathogenesis, how they hone to the target organ, and how they destroy their beta cell targets, causing clinical onset of T1D. The main goal of the research projects in my laboratory is to design and exploit tools for the manipulation of adaptive immunity for therapeutic purposes. To achieve this goal we use a variety of genetic, molecular biological, and biochemical approaches.. ...
Smith, H R.; Green, D; Raveche, E; Smathers, P; Gerson, R; and Steinberg, A D., "The induction of autoimmunity in normal mice. Abstr." (1982). Subject Strain Bibliography 1982. 2071 ...
Scu has an interesting post up expanding on his discussion of Luhmann and vulnerability yesterday. It seems that he want to draw a distinction between immunity and autoimmunity as it works in Derridas thought. Im not entirely following what hes trying to get at here. As I understand it, the idea is that in order…
Mellors, R C., "(slow) Virus infection, autoimmunity, and and lymphoma, an experimental model of human disease." (1969). Subject Strain Bibliography 1969. 1878 ...
Last week I talked some general issues about autoimmunity, and gave a brief background on NKT cells. Today Ill talk about the paper that spawned that discussion. ((Mattner, J., Savage, P., Leung, P., Oertelt, S., Wang, V., Trivedi, O., Scanlon, S., Pendem, K., Teyton, L., Hart, J. (2008). Liver Autoimmunity Triggered
From a lecture in Sweden autumn 2014 Dr. Suzanne Humphries speaks on vaccines and autoimmunity. Is there a connection between vaccination and asthma and allergy? Also, aluminium is used as an adjuvant, how does this affect the human body? More about Dr. Suzanne Humphries: http://drsuzanne.net/ THIS IS A NON PROFIT VIDEO PRODUCTION. ALL DONATIONS ARE APPRECIATED. PayPal: [email protected] THANK YOU ! Canal 2nd Opinion Sweden http://www.2op.se https://www.facebook.com/pages/Canal-2nd-Opinion/260569270754045
HOW TO PREVENT ALLERGIES, AUTOIMMUNITY AND CANCER IN HUMANS AND IN ANIMALS Todays toxic world contains many different harmful, health invaders, that it is
Wei, W.,Ming, X.,Yi, Z. Y.,et al. Autoimmunity Mediated Down-regulation Of B 2-adrenergic Receptor In COPD[J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE,2010,181 ...
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Infections and autoimmunity: the multifaceted relationship: http://www.jleukbio.org/content/87/3/385.full This article mentioned RNase L, as well as...
Turning to efficient autoimmunity testing, tools can have major impact on a physicians diagnostic decision, making an equally major difference in patient care.
Written by: Greg Ashby Have you ever wondered about autoimmunity? What is it, anyway? Chances are that you know someone affected - maybe that person i(...)
Citation Machine™ helps students and professionals properly credit the information that they use. Cite your film / online video in Journal of Autoimmunity format for free.
CD4+Foxp3+ regulatory T cells (Tregs) are known to control the progression of autoimmune diabetes, but when, where and how they exert their influence in this context are questions even now less than energetic controversy. afterwards. Interferon (IFN)- affected extensively on the gene-expression program of the local CD4+ effector cell population, unleashing it to aggressively attack the islets, and very HSP90AA1 crucial for the development of diabetes. Thus, Tregs rein in pancreatic autoimmunity through control of a central innate immune system player, NK cells. INTRODUCTION Foxp3+CD4+ Tregs Xanomeline oxalate manufacture regulate a variety of immune responses, including autoimmunity, allergy, inflammation, infection and tumorigenesis (Zheng and Rudensky, 2007; Sakaguchi et al., 2008). This cell population is required life-long to guard against autoimmunity, perhaps best illustrated by the multi-organ infiltrates that arise a few weeks after its acute ablation in adult mice (Kim et al., 2007). In ...
Onset and development of autoimmunity have been attributed to a number of factors, including genetic predisposition, age and different environmental factors. In this paper we discuss mathematical models of autoimmunity with an emphasis on two particular aspects of immune dynamics: breakdown of immune tolerance in response to an infection with a pathogen, and interactions between T cells with different activation thresholds. We illustrate how the explicit account of T cells with different activation thresholds provides a viable model of immune dynamics able to reproduce several types of immune behaviour, including normal clearance of infection, emergence of a chronic state, and development of a recurrent infection with autoimmunity. We discuss a number of open research problems that can be addressed within the same modelling framework.. ...
A patented type II collagen safely regulates the immune system, shielding delicate joint tissue from arthritic autoimmune attacks.
Scientists at Helmholtz Zentrum München have discovered a mechanism that amplifies the autoimmune reaction in an early stage of pancreatic islet autoimmunity prior to the progression to clinical type 1 diabetes. If the researchers blocked the corresponding molecules, the immune system was significantly less active. The study was conducted under the auspices of the German Center for Diabetes Research (DZD) and was published in the journal Science Translational Medicine. ...
Scientists at Helmholtz Zentrum München have discovered a mechanism that amplifies the autoimmune reaction in an early stage of pancreatic islet autoimmunity prior to the progression to clinical type 1 diabetes. If the researchers blocked the corresponding molecules, the immune system was significantly less active. The study was conducted under the auspices of the German Center for Diabetes Research (DZD) and was published in the journal Science Translational Medicine. ...
In certain plant hybrids, immunity signaling is initiated when immune components interact in the absence of a pathogen trigger. In Arabidopsis thaliana, such autoimmunity and cell death are linked to variants of the NLR RPP7 and the RPW8 proteins involved in broad-spectrum resistance. We uncover the molecular basis for this autoimmunity and demonstrate that a homolog of RPW8, HR4 Fei-0, can trigger the assembly of a higher-order RPP7 complex, with autoimmunity signaling as a consequence. HR4 Fei-0-mediated RPP7 oligomerization occurs via the RPP7 C-terminal leucine-rich repeat (LRR) domain and ATP-binding P-loop. RPP7 forms a higher-order complex only in the presence of HR4 Fei-0 and not with the standard HR4 variant, which is distinguished from HR4 Fei-0 by length variation in C-terminal repeats. Additionally, HR4 Fei-0 can independently form self-oligomers, which directly kill cells in an RPP7-independent manner. Our work provides evidence for a plant resistosome complex and the mechanisms by ...
In certain plant hybrids, immunity signaling is initiated when immune components interact in the absence of a pathogen trigger. In Arabidopsis thaliana, such autoimmunity and cell death are linked to variants of the NLR RPP7 and the RPW8 proteins involved in broad-spectrum resistance. We uncover the molecular basis for this autoimmunity and demonstrate that a homolog of RPW8, HR4 Fei-0, can trigger the assembly of a higher-order RPP7 complex, with autoimmunity signaling as a consequence. HR4 Fei-0-mediated RPP7 oligomerization occurs via the RPP7 C-terminal leucine-rich repeat (LRR) domain and ATP-binding P-loop. RPP7 forms a higher-order complex only in the presence of HR4 Fei-0 and not with the standard HR4 variant, which is distinguished from HR4 Fei-0 by length variation in C-terminal repeats. Additionally, HR4 Fei-0 can independently form self-oligomers, which directly kill cells in an RPP7-independent manner. Our work provides evidence for a plant resistosome complex and the mechanisms by ...
There are many physicians who are witnessing an increasing number of children with complex inflammatory & autoimmune conditions, and are beginning to suspect that vaccines may be playing more of a contributing role in the development of these conditions, than what they were previously led to believe. Nonetheless, these physicians dont have a safe forum in which they can discuss their concerns. This film, "THE GREATER GOOD," may be the appropriate medium through which physicians can begin to open up the next phase of dialogue about their growing concerns of vaccine safety & efficacy. ...
Studies in type 1 diabetes indicate potential disease heterogeneity, notably in the rate of β-cell loss, responsiveness to immunotherapies and, in limited studies, islet pathology. We sought evidence for different immunological phenotypes using two approaches. First, we defined blood autoimmune response phenotypes by combinatorial, multi-parameter analysis of autoantibodies and autoreactive T-cell responses in 33 children/adolescents with newly-diagnosed disease. Multi-dimensional cluster analysis showed two equal-sized patient agglomerations, characterized by pro-inflammatory (IFN-γ+, multi-autoantibody-positive) and partially-regulated (IL-10+, pauci-autoantibody-positive) responses. Multi-autoantibody-positive non-diabetic siblings at high-risk of disease progression showed similar clustering. Second, pancreas samples obtained post mortem from a separate cohort of 21 children/adolescents with recently-diagnosed type 1 diabetes were examined immunohistologically. This revealed two distinct ...
https://m.medicalxpress.com/news/2017-05-trigger-autoimmune-disease.html Trigger for autoimmune disease identified May 11, 2017 [IMG] Researchers...
The lecture will be based on the recent book An Epidemic of Absence - A New Way of Understanding Allergies and Autoimmune Disease by Moises Velasquez-Manoff. I...
Speaker:MarkM.Davis,StandfordInstituteforImmunology,TransplantationandInfectionTime:14:30,Thursday,November9,2017Venue:Room705,ComprehensiveBuilding,SchoolofMedicine,ZijingangCampus
Before I knew I was the proud owner of an immune system that couldnt tell self from invader, doctors pushed sedatives on me. They hypothesized that my buffet of bodily dysfunctions - stabbing pain around my lungs, clawed hands, ruddy and hot joints - were provoked by overwork and exams, stress or anxiety. Something of my…
Before I knew I was the proud owner of an immune system that couldnt tell self from invader, doctors pushed sedatives on me. They hypothesized that my buffet of bodily dysfunctions - stabbing pain around my lungs, clawed hands, ruddy and hot joints - were provoked by overwork and exams, stress or anxiety. Something of my…
We walk a fine line between death due to immune deficiency, smothered under the weight of pathogens and parasites, and death by hyperimmunity, eaten alive by
Can you pick the Transplantation and more!? Test your knowledge on this science quiz to see how you do and compare your score to others. Quiz by cgunn911
ANTI MALARIAL DRUGS Anti malarial drugs have been used for the treatment of SLE and RA since the early 1900s. The precise mechanism of action remains uncertain, but they have been shown to inhibit cytokine (IL-1 and IL-6) production in vitro. The anti malarial pass freely through cell membranes at neutral pH, but in…
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Ongoing research is generating data collected from its users to improve the product.. These examples show three different approaches to building this market. Lumosity began with an engaging front end and is now enriching the data back end. Brain Resource began with data and is adapting their training for the corporate health and wellness market. Cognifit is a hybrid, using its initial data to create products for the professional market but with consumers targeted through providers.. Can these collective new data sources for brain training ignite a growing market for personalized learning?. ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Were on the show today with Dr. Amy Myers, MD, New York Times bestselling author of The Autoimmune Solution and a leader in Functional Medicine. On this show, we dig into the causes, prevention, and healing of autoimmune issues that you might not even realize you have-but suffer with every day! Learn More ...
Autoimmunity, Disease, Antibody Production, Antibody Responses, Attention, Cell, Cell Differentiation, Cells, Environment, Immune System, Infection, Infectious Disease, Literature, Play, Production, Risk, Role, Understanding, Antigen, Arthritis
Autoimmunità nella dermatite atopica: biomarcatore o semplicemente epifenomeno? legando anticorpi IgE o attivando le cellule T Autoimmunity in atopic.
2018 Award Winners at the International Congress of Autoimmunity (in the middle from left to right): JOSHUA OOI, Australia, GERHARD KRÖNKE, Austria, GABRIEL J. TOBÓN, France. The award ceremony for the MAI Award 2018 was held during the Autoimmunity 2018 congress in Lisbon ​in May, and the winner was asked to speak at a plenary session. Selection for this bi-annual award has been made by an International Scientific Committee comprised of well established authorities within the autoimmunity disease fields to encourage progress in autoimmunity research. Award 2016. Carlo Perricone, was awarded first prize for the Mosaic of Autoimmunity, MAI Award 2016 at the 10th International Congress of Autoimmunity in Leipzig, Germany ...
Our study provides the first evidence, to our knowledge, that B7-H1 nearly abolishes TH17 lineage differentiation of murine and human CD4+ T cells and hence controls T cell-mediated CNS autoimmunity.. Several lines of evidence point to a novel PD-1-independent effect of B7-H1-Ig during TH17 differentiation. First, we blocked interaction of B7-H1-Ig with murine or human PD-1 using a PD-1 binding Ab and found no interference with the anti-TH17 effect. Second, the completely preserved effect of B7-H1-Ig on TH17 differentiation using PD-1KO T cells provides unequivocal evidence that, at least in the murine system, this effect is not mediated via PD-1. Although the presence of a non-PD receptor for B7-H1 based on molecular modeling and functional mapping has been suggested before (12, 39), our study now provides clear experimental evidence of non-PD-1-mediated effects by B7-H1. Recently, B7.1 was identified as another receptor for B7-H1 on T cells (40), but in our setup, involvement of B7.1 could ...
The findings, published in Diabetes, ​examined the association between plasma levels of vitamin D -measured as 25-hydroxyvitamin D (25[OH]D) concentration - and islet autoimmunity(IA), which has been implicated in the development and progression of type 1 diabetes.. "For several years there has been controversy among scientists about whether vitamin D lowers the risk of developing of islet autoimmunity and type 1 diabetes," ​commented lead author Dr Jill Norris from the Colorado School of Public Health.. Type 1 diabetes is a chronic autoimmune disease that is now the most common metabolic disorder in children under age 10 and it increasing by between 3% and 5% annually worldwide.. While it has long been known that islet autoimmunity - which occurs when the immune system attacks the islet cells in the pancreas that produce insulin - is a precursor to type 1 diabetes, evidence for the suggestion that vitamin D levels may play a role in the development of this autoimmunity, and therefore the ...
The Autoimmunity Bible & Norton Protocol is definitely an online package of five complete The Autoimmunity Bible & Norton Protocol. The type of material mentioned are all cheap and you will find many in your house. The instructions are all well organized and developed in simple language. The following requirement is usually to access research materials. We now have done nearly all of it in your case for The Autoimmunity Bible & Norton Protocol. Exhibits and graphs are positioned for you personally. Your work will probably be perfect as well as through Autoimmunity Bible & Norton Protocol. Youll be appreciated and you will be ranked high. One and only thing you have to look into will be the written part. To the you have plenty of time that you simply stored in other details. Thus The Autoimmunity Bible & Norton Protocol will likely be perfect in every sense and you can relax. All of this you enjoy for a nominal amount. No recourse, no burden.. via: www.thebestitems.com. ...
An appropriate balance between inflammatory and regulatory T cells is critical to maintaining immune homeostasis and preventing autoimmune diseases, including m...
Several genes within a syntenic region of human and mouse chromosome 1 are associated with predisposition to systemic lupus erythematosus. Analyses of lupus-prone congenic mice have pointed to an important role for the signaling lymphocyte activation molecule family (slamf)6 surface receptor in lupus pathogenesis. In this paper, we demonstrate that a second member of the Slamf gene family, Slamf4 (Cd244), contributes to lupus-related autoimmunity. B6.Slamf4−/− mice spontaneously develop activated CD4 T cells and B cells and increased numbers of T follicular helper cells and a proportion develop autoantibodies to nuclear Ags. B6.Slamf4−/− mice also exhibit markedly increased autoantibody production in the B6.C-H-2bm12/KhEg → B6 transfer model of lupus. Although slamf4 function is best characterized in NK cells, the enhanced humoral autoimmunity of B6.Slamf4−/− mice is NK cell independent, as judged by depletion studies. Taken together, our findings reveal that slamf4 has an NK ...
Our results support the concept that variants in CTLA4 provide the basis for a novel Mendelian form of early-onset CD associated with systemic autoimmunity. Incomplete penetrance of autoimmunity further indicates the presence of other genetic and/or environmental modifiers.A novel missense variant was identified in CTLA4 encoding CTLA-4, a coinhibitory protein expressed by T cells and required for regulation of T cell activation. The residue affected by the mutation, CTLA-4 Tyr60, is evolutionarily highly conserved, and the identified Y60C variant is predicted to affect protein folding and structural stability and demonstrated to cause impaired CTLA-4 dimerisation and CD80 binding. Intestinal inflammation and autoimmunity in carriers of CTLA-4 Y60C exhibit incomplete penetrance with a spectrum of clinical presentations ranging from asymptomatic carrier status to fatal autoimmunity and intestinal inflammation. In a clinically affected CTLA-4 Y60C carrier, T cell proliferation was increased in ...
The prevalence of autoimmunity in America is growing. There are now well over 100 different autoimmune diseases, and an estimated 50 million Americans have an autoimmune disorder ranging from Crohns disease, Irritable Bowel Syndrome (IBS), Hashimotos disease, ulcerative colitis, Multiple Sclerosis (MS), fibromyalgia or rheumatoid arthritis1. In general, autoimmunity is a dysfunctional immune response where our immune system attacks our healthy cells2. Any disease that results from this attack is an autoimmune disease. Because an autoimmune response can be directed toward any cell/tissue/organ, there can be hundreds of autoimmune diseases3. In almost all cases of autoimmunity, the conventional treatments are potent steroids and other drugs that suppress the immune system to relieve the symptoms4. These treatments come with a significant risks or side effects while not correcting the underlying cause of the immune system dysfunction5. Modern research is making it pretty clear that no matter ...
Most autoreactive T cells are exposed to self-antigen either in the thymus or the periphery, and high avidity T cells are eliminated in both compartments. In contrast, lower avidity T cells are often found in ongoing autoimmune diseases (Bulek et al., 2012) and in anti-tumor responses (McMahan and Slansky, 2007). Thus, expression of a low avidity TCR, allowing autoreactive T cells to bypass elimination, is a major mechanism by which autoreactive T cells escape tolerance (von Herrath et al., 1994; Nugent et al., 2000; Zehn and Bevan, 2006). However, up to this point, we had limited insight into the phenotypic and functional characteristics of these low avidity self-reactive T cells. Thus, it was unclear how self-antigen recognition in the thymus or periphery impacts the function of these T cells and whether such exposure imprinted mechanisms that restrict their activation. The failure to negatively select low avidity self-reactive T cells stimulated us to study how well these T cells respond to ...
Do you have crud in the blood? Millions of people suffer from autoimmunity whether they know it or not. The root cause of most weight gain, brain and mood problems, and fatigue, autoimmunity can take years--or even decades--for symptoms and a clear diagnosis to arise. Through years of research, Dr. Tom OBryan has discovered that autoimmunity is actually a spectrum, and many people experiencing general malaise are already on it. And while autoimmune diseases, such as Alzheimers, Multiple Sclerosis, osteoporosis, diabetes, and lupus, have become the third leading cause of death behind heart disease and cancer, many people affected are left in the dark. The good news is that many autoimmune conditions can be reversed through a targeted protocol designed to heal the autoimmune system, 70 percent of which is located in the gut. The Autoimmune Fix includes two comprehensive 3-week plans: In the first 3 weeks, youll follow a Paleo-inspired diet during which you cut out gluten, sweets, and dairy--the ...
The study of rare phenotypes has a long history in the description of autoimmune disorders. First Mendelian syndromes of idiopathic tissue destruction were defined more than one hundred years ago and were later revealed to result from immune-mediated reactivity against self. In the past two decades, continuous advances in sequencing technology and particularly the advent of next generation sequencing have allowed to define the genetic basis of an ever-growing number of Mendelian forms of autoimmunity. This has provided unique insight into the molecular pathways that govern immunological homeostasis and that are indispensable for the prevention of self-reactive immune-mediated tissue damage and horror autotoxicus. Here, we will discuss selected examples of past and recent investigations into rare phenotypes of autoimmunity that have delineated pathways critical for central and peripheral control of the adaptive immune system. We will outline the implications of these findings for rare and ...
Re-framing the Theory of Autoimmunity in the Era of the Microbiome: Persistent Pathogens, Autoantibodies, and Molecular Mimicry. The theory of autoimmunity was developed at a time when the human body was regarded as largely sterile. Antibodies in patients with chronic inflammatory disease could consequently not be tied to persistent human pathogens. The concept of the "autoantibody" was created to reconcile this phenomenon. Today, however, the discovery of the human microbiome has revolutionized our understanding of human biology. Humans are superorganisms that harbor trillions of persistent microbial cells. Indeed, vast human microbiomes have been detected in human tissue and blood. These microbial ecosystems harbor thousands of newly identified bacteria, viruses, and other microorganisms - most of which can act… (read full paper). ...
Although current thinking has focused on genetic variation between individuals and environmental influences as underpinning susceptibility to both autoimmunity and cancer, an alternative view is that human susceptibility to these diseases is a consequence of the way the immune system evolved. It is important to remember that the immunological genes that we inherit and the systems that they control were shaped by the drive for reproductive success rather than for individual survival. It is our view that human susceptibility to autoimmunity and cancer are the evolutionarily acceptable side effects of the immune adaptations that evolved in early placental mammals to accommodate a fundamental change in reproductive strategy. Studies of immune function in mammals shows that high affinity antibodies and CD4 memory, along with its regulation, co-evolved with placentation. By dissection of the immunologically active genes and proteins that evolved to regulate this step change in the mammalian immune system,
Dr. Kim Simpfendorfer completed her undergraduate degrees and PhD at the University of Melbourne in the Department of Microbiology and Immunology, in Melbourne Australia. Her PhD studies focused on the mucosal immune system and particularly on the presence of antibodies that function to protect the bodys mucosal surfaces. She also studied secreted mucosal antibodies in the context of interactions between the environment and the development of autoimmune diseases such as Type 1 Diabetes.. Kim joined the Robert S. Boas Center for Genomics and Human genetics in 2010 as a Postdoctoral Fellow to work with Dr. Peter K. Gregersen on the functional genetics of human autoimmunity. Kim served as the Secretary of the Young Investigators Society at the Feinstein Institute from August 2014 until September 2015.. ...
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If youve been diagnosed with an autoimmune disease, your doctor probably told you that there is no cure, it will continue to get worse, and the only treatment option is a powerful medication that suppresses your immune system (and has really bad side effects). That probably made you feel scared, helpless, and depressed. Like your life is over. But you do not need to resign yourself to this fate. You have other treatment options and you can feel better. You simply need an integrative approach to autoimmunity. Whether you have Hashimotos, ankylosing spondylitis, multiple sclerosis, Crohns disease, or rheumatoid arthritis, an integrative approach to autoimmunity can help you heal.
Autoimmunity is an abnormal biological process that can lead to pathological disease. It is caused when an immune system that normally recognises and destroys foreign invaders such as viruses and bacteria, ceases to recognise its own tissues as "self" and attacks them causing the breakdown of structures and biological processes necessary for health. These degenerative processes can affect specific cells within the body as in Type 1 autoimmune diabetes where cells of the immune system infiltrate the pancreas and destroy the cells that produce insulin. Autoimmune processes can also be tissue specific such as in the disease Myasthenia gravis. In this disease antibodies, (specifically produced proteins of the immune system) bind to and block receptors in muscle that cause progressive muscle weakening. In the case of Systemic Lupus Erythamatosus the autoimmune process is more general in nature and can attack many different tissues causing a variety of symptoms including rashes, kidney damage, and ...
Published: 16 Feb 2016 , Last Updated: 16 Feb 2016 13:29:57 An article by RVC researchers has been published in Journal of Immunology. In this work, RVC researchers set about to understand microRNA regulation of helper T cells development. MicroRNAs, as their name implies, are small RNAs that provide an essential regulation of gene expression by controlling translation of protein expressing messenger RNAs. Previously it was known that microRNAs were important for the development of a subset of helper T cells called regulatory T cells, which are required to regulate the immune response and prevent attacks against host tissue that lead to autoimmunity. In this article the researchers describe their identification of important individual microRNAs and relevant genes they regulate to control regulatory T cell development. Therefore, through this work the researchers have identified a novel way of regulating helper T cell development and controlling the immune response. This article has been recently ...
Published: 16 Feb 2016 , Last Updated: 16 Feb 2016 13:29:57 An article by RVC researchers has been published in Journal of Immunology. In this work, RVC researchers set about to understand microRNA regulation of helper T cells development. MicroRNAs, as their name implies, are small RNAs that provide an essential regulation of gene expression by controlling translation of protein expressing messenger RNAs. Previously it was known that microRNAs were important for the development of a subset of helper T cells called regulatory T cells, which are required to regulate the immune response and prevent attacks against host tissue that lead to autoimmunity. In this article the researchers describe their identification of important individual microRNAs and relevant genes they regulate to control regulatory T cell development. Therefore, through this work the researchers have identified a novel way of regulating helper T cell development and controlling the immune response. This article has been recently ...
Our lab works in the broad fields of T cell differentiation and tolerance/autoimmunity, translating mechanistic studies on mouse models to normal and diseased humans. Studies on T cell differentiation focus on maturation and selection of the T cell repertoire in the thymus, and on cellular and molecular influences on the "flavor" of T cell responses in the periphery. Studies on autoimmunity explore the immunological mechanisms of type-1 diabetes, rheumatoid arthritis and APECED, in particular central and peripheral mechanisms of T cell tolerance. Major questions tackled are what initiates these diseases, how is their progression regulated, what are the final effector mechanisms, and how do genetic and environmental factors impact disease unfolding. Current foci include: the Aire transcriptional regulatory molecule, Foxp3-expressing Treg cells, immunometabolism and gut microbiota. The application of computational and bioinformatic strategies to these and other issues is one of the labs ...
Thousands of genetic variants have been identified, which contribute to the development of complex diseases, but determining how to elucidate their biological consequences for translation into clinical benefit is challenging. Conflicting evidence regarding the functional impact of genetic variants in the tyrosine kinase 2 (TYK2) gene, which is differentially associated with common autoimmune diseases, currently obscures the potential of TYK2 as a therapeutic target. We aimed to resolve this conflict by performing genetic meta-analysis across disorders; subsequent molecular, cellular, in vivo, and structural functional follow-up; and epidemiological studies. Our data revealed a protective homozygous effect that defined a signaling optimum between autoimmunity and immunodeficiency and identified TYK2 as a potential drug target for certain common autoimmune disorders.
MPH - The Healing Power of Essential Oils: Soothe Inflammation, Boost Mood, Prevent Autoimmunity, and Feel Great in Every Way ISBN - 9781524761363 ...
AUTOIMMUNITY and HEMATURIA related symptoms, diseases, and genetic alterations. Get the complete information with our medical search engine for phenot
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TY - JOUR. T1 - Biomedicine. T2 - A gender gap in autoimmunity. AU - Whitacre, Caroline C.. AU - Reingold, Stephen C.. AU - OLooney, Patricia A.. AU - Blankenhorn, Elizabeth. AU - Brinley, Floyd. AU - Collier, Elaine. AU - Duquette, Pierre. AU - Fox, Howard. AU - Giesser, Barbara. AU - Gilmore, Wendy. AU - Lahita, Robert. AU - Lee Nelson, J.. AU - Reiss, Carol. AU - Riskind, Peter. AU - Voskuhl, Rhonda. PY - 1999/2/26. Y1 - 1999/2/26. UR - http://www.scopus.com/inward/record.url?scp=0033604943&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0033604943&partnerID=8YFLogxK. U2 - 10.1126/science.283.5406.1277. DO - 10.1126/science.283.5406.1277. M3 - Short survey. C2 - 10084932. AN - SCOPUS:0033604943. VL - 283. SP - 1277. EP - 1278. JO - Science. JF - Science. SN - 0036-8075. IS - 5406. ER - ...
Eventbrite - Dr. K presents The 6 Commonly Overlooked Causes of Autoimmunity - Tuesday, 30 January 2018 at True Wellness Integrative Health Centre, Kitchener, ON. Find event and ticket information.
Eventbrite - Dr. K presents The 6 Commonly Overlooked Causes of Autoimmunity - Tuesday, 9 January 2018 at True Wellness Integrative Health Centre, Kitchener, ON. Find event and ticket information.
Our study shows that islet autoimmunity is considerably less common among type 2 diabetic individuals of Punjabi ancestry in Birmingham, U.K., than in those of white Caucasian origin. The differences observed between the two ethnic groups may reflect both the higher prevalence of classical type 2 diabetes in South Asians and their lower susceptibility to autoimmune disease. The overall prevalence of islet autoantibodies among the individuals diagnosed with type 2 diabetes in our study cohort (2.6%) was significantly lower than that observed in the pilot study (27%), as was the frequency in the control group (3.9 compared with 9%, respectively) (2). The reasons for these differences are unclear, as both methods were approved by the Diabetes Antibody Standardization Programme (10). The most likely explanation is that the high prevalence of autoimmunity observed in the pilot study is a spurious result due to the small number of individuals investigated (33 type 2 diabetic and 98 control subjects). ...
It has long been thought that viruses play a part in the development of chronic inflammatory diseases, especially autoimmunity. Many healthcare practitioners report there is frequently a hidden infection that either precedes or seems to trigger an initial autoimmune attack, or subsequently appears when the immune system is weakened once autoimmunity is activated.. This creates a vicious cycle of infection and illness. Infections are opportunistic and often travel together - many autoimmune patients find they host multiple infections that are bacterial, viral, parasitic and/or fungal, driving the inflammation that leads to symptoms.. The relationship between viral infection and autoimmune disease is multifaceted, involving numerous complex processes in the body. Scientists believe that a variety of factors must usually be present for an infection to result in an autoimmune condition. This includes not only a genetic predisposition but also lifestyle and environmental factors such as:. ...
In this study, we explore the function of LRP1 expression in myeloid cells during MS using the mouse model EAE. To begin, we have made the novel observation that LRP1 protein expression is significantly increased in human MS lesions, compared to normal appearing brain tissue. The cellular compartments involved in the increase of LRP1 immunoreactivity included the myeloid cells and astrocytes. This observation is in agreement with our previous work showing that LRP1 expression is upregulated during EAE [11] and the work of Hendrickx et al., showing that LRP1 transcript is increased at the rim of MS lesions [41]. The LRP1 expression increase by glia is not limited to MS, as previous work has demonstrated a similar pattern during CNS injury and neoplasia [42]. Therefore, although our study centered on LRP1 function in myeloid cells, future studies will be needed to understand the role of LRP1 in astrocytes.. Here, we have explored the contribution of LRP1 expression during EAE in two distinct ...
The prevalence of autoimmune diseases are increasing at a rapid rate and now affect 1 in 4 women and 1 in 6 men.. Over 80 autoimmune diseases have been identified and in this health talk, Amanda will discuss some of the current hypotheses around the possible causative factors. Amanda will also look at some of the most researched nutrients and dietary modifications that have shown long-lasting impact on the progression of autoimmune mechanisms.. Amanda has been in private practice for 21 years and has treated hundreds of individuals with autoimmune conditions, ranging from coeliac disease to multiple sclerosis.. Dont miss this opportunity to learn more about health from our clinic director.. DATE: Monday 1st May at the clinic. TIME: 6:30pm Talk will run for 30 minutes + opportunity to ask questions. To reserve your place please call or email reception on (02) 9555 8806 or [email protected] ...
The incidence of type 1 diabetes has risen considerably in the past 30 years due to changes in the environment that have been only partially identified. In this Series paper, we critically discuss candidate triggers of islet autoimmunity and factors thought to promote progression from autoimmunity to overt type 1 diabetes. We revisit previously proposed hypotheses to explain the growth in the incidence of type 1 diabetes in light of current data. Finally, we suggest a unified model in which immune tolerance to β cells can be broken by several environmental exposures that induce generation of hybrid peptides acting as neoautoantigens.. ...
This gene encodes an enzyme belonging to the glucose-6-phosphatase catalytic subunit family. These enzymes are part of a multicomponent integral membrane system that catalyzes the hydrolysis of glucose-6-phosphate, the terminal step in gluconeogenic and glycogenolytic pathways, allowing the release of glucose into the bloodstream. The family member encoded by this gene is found in pancreatic islets and does not exhibit phosphohydrolase activity, but it is a major target of cell-mediated autoimmunity in diabetes. Several alternatively spliced transcript variants of this gene have been described, but their biological validity has not been determined. [provided by RefSeq, Jul 2008 ...
If there is any doubt in anybodys mind about the role of estrogen as a cause of autoimmune conditions I hope that his will clarify the situation some...
In light of the discovery of Autoimmune Syndrome Induced by Adjuvants, or ASIA, Vaccines and Autoimmunity explores the role of adjuvants - specifically aluminum in different vaccines - and how they can induce diverse autoimmune clinical manifestations in genetically prone individuals. Vaccines and Autoimmunity is divided into three sections; the first contextualizes the role of adjuvants in the framework of autoimmunity, covering the mechanism of action of adjuvants, experimental models of adjuvant induced autoimmune diseases, infections as adjuvants, the Gulf War Syndrome, sick-building syndrome (SBS), safe vaccines, toll-like receptors, TLRS in vaccines, pesticides as adjuvants, oil as adjuvant, mercury, aluminum and autoimmunity. The following section reviews literature on vaccines that have induced autoimmune conditions such as MMR and HBV, among others. The final section covers diseases in which vaccines were known to be the solicitor - for instance, systemic lupus erythematosus - and ...
PROBLEM: The aim of this study was to verify whether anti-thyroid antibodies are present in the follicular milieu of euthyroid infertile women with thyroid autoimmunity undergoing in vitro fertilization (IVF) and whether IVF outcome is different in affected women with respect to negative controls. A secondary endpoint was to check whether there are changes in thyroid hormone levels during the IVF cycle. METHOD OF STUDY: Anti-thyroglobulin and anti-thyroperoxidase levels were measured in both follicular fluid and serum on the day of oocyte retrieval in women with thyroid autoimmunity. Serum TSH, FT3, and FT4 levels were measured in all patients before treatment initiation, on the day of oocyte retrieval and of pregnancy test. IVF outcome parameters were recorded in all women. RESULTS: Oocyte fertilization, grade A embryos, and pregnancy rates were lower in women with thyroid autoimmunity than in negative controls, while early miscarriage rate was higher. Anti-thyroid antibodies were measurable in ...
Title:Targeting Chemokine (C-X-C motif) Receptor 3 in Thyroid Autoimmunity. VOLUME: 8 ISSUE: 2. Author(s):Poupak Fallahi, Silvia Martina Ferrari, Alda Corrado, Dilia Giuggioli, Clodoveo Ferri and Alessandro Antonelli. Affiliation:Department of Clinical and Experimental Medicine, University of Pisa, Via Savi, 10, I-56126, Pisa, Italy.. Keywords:CXCL9, CXCL10, CXCL11, CXCR3, Graves disease, thyroid autoimmunity, thyroid autoantibodies, thyroiditis.. Abstract:The C-X-C chemokine receptor (CXCR)3 and its chemokines (CXCL9, CXCL10, CXCL11) are involved in the pathogenesis of autoimmune thyroiditis (AT), Graves disease (GD) and Graves Ophthalmopathy (GO). Under the influence of interferon(IFN)γ, the IFNγ-induced protein 10 (IP-10/CXCL10) is secreted by thyrocytes, orbital fibroblasts and preadipocytes. In tissue, Th1 lymphocytes are recruited; hence IFNγ is enhanced, which stimulates CXCL10 secretion reiterating the autoimmune process. The presence of elevated levels of CXCL10 in peripheral ...
When you think about it, the job that the immune system does in protecting us is simply incredible. We are constantly being exposed to different pathogens, toxins, and food allergens, and our immune system does an amazing job of making sure these factors dont cause us any harm, while at the same time differentiating self from non-self. There are numerous regulatory mechanisms which help to maintain immune homeostasis and prevent the development of autoimmune thyroid conditions such as Graves Disease and Hashimotos Thyroiditis. And one of the main components of the immune system which helps to prevent autoimmunity is the regulatory T cells.. Maintaining self-tolerance while at the same time mounting immune responses against pathogens is a complex process. Regulatory T cells (Tregs) are widely regarded as the primary mediators of peripheral tolerance (1). Tregs originate in the thymus, although they also can derive from peripheral CD4+ T cells (2). A healthy immune system will have an abundance ...
Objectives: Celiac disease (CD) is associated with thyroid autoimmunity and other autoimmune diseases. Data are, however, lacking regarding the relationship between thyroid autoimmunity and thyroid function, especially in regard to CD. Our aim was to investigate the impact of thyroid autoimmunity on thyroid function in 12-year-old children with CD compared to their healthy peers. Methods: A case-referent study was conducted as part of a CD screening of 12-year-olds. Our study included 335 children with CD and 1695 randomly selected referents. Thyroid autoimmunity was assessed with antibodies against thyroid peroxidase (TPOAb). Thyroid function was assessed with thyroid-stimulating hormone and free thyroxine. Results: TPOAb positivity significantly increased the risk of developing hypothyroidism in all children. The odds ratios (with 95% confidence intervals) were 5.3 (2.7-11) in healthy 12-year-olds, 10 (3.2-32) in screening-detected CD cases, 19 (2.6-135) in previously diagnosed CD cases, and ...
In the past decade, the suppressive effects, mainly through the secretion of IL-10, of regulatory B cells on inflammatory responses have been reported in a variety of immune disorders (33-36). Additionally, immune regulation through the interaction of immune cells with the intrinsic phenotype of regulatory B cells (e.g., CD1dhiCD5+, T2-MZP, Tim-1+, and CD9+) were demonstrated in various diseases, and it plays a critical role in autoimmune diseases (37). In recent studies, functional studies in cancer diseases are emerging (38-40). In particular, the change of the distribution of regulatory B cells in cancer tissue is considered to one of important indicators (8-10). Emerging evidence suggests that regulatory B cells suppress effector immune cells including IFN-γ-producing cytotoxicity cells in various cancer diseases through the secretion of IL-10 (11). Although regulatory B cells have to play the suppressive role on the effector function of T cells in autoimmune diseases to cure diseases (41), ...
Autoantibodies to transglutaminase 2 (TG2) are hallmarks of celiac disease. To address B cell tolerance and autoantibody formation to TG2, we generated immunoglobulin knock-in (Ig KI) mice that express a prototypical celiac patient-derived anti-TG2 B cell receptor equally reactive to human and mouse TG2. We studied B cell development in the presence/absence of autoantigen by crossing the Ig KI mice to Tgm2−/− mice. Autoreactive B cells in Tgm2+/+ mice were indistinguishable from their naive counterparts in Tgm2−/− mice with no signs of clonal deletion, receptor editing, or B cell anergy. The autoreactive B cells appeared ignorant to their antigen, and they produced autoantibodies when provided T cell help. The findings lend credence to a model of celiac disease where gluten-reactive T cells provide help to autoreactive TG2-specific B cells by involvement of gluten-TG2 complexes, and they outline a general mechanism of autoimmunity with autoantibodies being produced by ignorant B cells on ...
Dysfunction within the endocrine system can lead to a variety of diseases with autoimmune attack against individual components being some of the most common. Endocrine autoimmunity encompasses a spectrum of disorders including, e.g., common disorders such as type 1 diabetes, Graves disease, Hashimotos thyroiditis, and rarer disorders including Addisons disease and the autoimmune polyendocrine syndromes type 1 (APS 1) and type 2 (APS 2) (see Table 1.6.1). Autoimmune attack within each of these diseases although aimed at different endocrine organs is caused by a breakdown in the immune systems ability to distinguish between self and nonself antigens, leading to an immune response targeted at self tissues. Investigating the mechanisms behind this breakdown is vital to understand what has gone wrong and to determine the pathways against which therapeutics can be targeted. Before discussing how self-tolerance fails, we first have to understand how the immune system achieves self-tolerance. ...
செயற்படுதல்: நோயெதிர்ப்புத் திறன் · தன்னெதிர்ப்பு (Autoimmunity) · மாற்றுநோயெதிர்ப்புத் திறன் (Alloimmunity) · ஒவ்வாமை · ...
Glycans in the immune system and The Altered Glycan Theory of Autoimmunity. J Autoimmun. 2015, 57 (6): 1-13. PMC 4340844. PMID ... Mucosal-associated invariant T cells in autoimmunity, immune-mediated diseases and airways disease. Immunology. May 2016, 148 ( ...
"Journal of Autoimmunity. 34 (3): J247-57. doi:10.1016/j.jaut.2009.11.011. PMC 2835849. PMID 20018479.. ...
However, there is little evidence linking chronic Chikungunya virus disease and the development of autoimmunity. ...
2008). "Clinical spectrum of voltage-gated potassium channel autoimmunity". Neurology. 70 (20): 1883-90. doi:10.1212/01.wnl. ...
A long-standing H. pylori infection may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies ... Banka S, Ryan K, Thomson W, Newman WG (June 2011). "Pernicious anemia - genetic insights". Autoimmunity Reviews. 10 (8): 455-9 ... Intrinsic Factor Secretion, Vitamin B12 Absorption and Genetic Aspects of Gastric Autoimmunity". British Journal of Haematology ...
Toivanen P, Toivanen A (1994). "Does Yersinia induce autoimmunity?". International Archives of Allergy and Immunology. 104 (2 ... Tomer Y, Davies TF (February 1993). "Infection, thyroid disease, and autoimmunity". Endocrine Reviews. 14 (1): 107-20. doi: ... Menconi F, Marcocci C, Marinò M (2014). "Diagnosis and classification of Graves' disease". Autoimmunity Reviews. 13 (4-5): 398- ... and was hypothesized to contribute to the development of thyroid autoimmunity arising for other reasons in genetically ...
Also, unlike alemtuzumab, cladribine is not associated with secondary autoimmunity.[38] This is probably due to the fact ... is thought to explain the lack of secondary autoimmunity. ...
... and autoimmunity". ILAR Journal. 45 (3): 278-91. doi:10.1093/ilar.45.3.278. PMID 15229375.. ...
Michael's Hospital in Toronto.[1] Its Arthritis & Autoimmunity Research Centre was transferred to the University Health Network ...
Borrello S, Nicolò C, Delogu G, Pandolfi F, Ria F (2011). "TLR2: a crossroads between infections and autoimmunity?". ...
Glycans in the immune system and The Altered Glycan Theory of Autoimmunity. J Autoimmun. 2015, 57 (6): 1-13. PMID 25578468. doi ...
Autoimmunity. 35 (5): 335-41. doi:10.1080/0891693021000005402. PMID 12515288.. ...
"Overexpression of the Cytokine BAFF and Autoimmunity Risk". New England Journal of Medicine. 46 (17): 1615-26. doi:10.1056/ ...
Butler MH, Hayashi A, Ohkoshi N, Villmann C, Becker CM, Feng G, De Camilli P, Solimena M (2000). "Autoimmunity to gephyrin in ...
Journal of Autoimmunity. 2010-08, roč. 35, čís. 1, s. 86-97. Dostupné online [cit. 2019-02-04]. ISSN 0896-8411. DOI:10.1016/j. ...
"Journal of Autoimmunity. 57: 1-13. doi:10.1016/j.jaut.2014.12.002. PMC 4340844. PMID 25578468.. ... "Glycans in the immune system and The Altered Glycan Theory of Autoimmunity: a critical review" ...
Different virus families have different levels of ability to alter their genomes and trick the immune system into not recognizing. Some viruses have relatively unchanging genomes like paramyxoviruses while others like influenza have rapidly changing genomes that inhibit our ability to create long lasting vaccines against the disease. Viruses in general have much faster rate of mutation of their genomes than human or bacterial cells. In general viruses with shorter genomes have faster rates of mutation than longer genomes since they have a faster rate of replication.[15] It was classically thought that viruses with an RNA genome always had a faster rate of antigenic variation than those with a DNA genome because RNA polymerase lacks a mechanism for checking for mistakes in translation but recent work by Duffy et al. shows that some DNA viruses have the same high rates of antigenic variation as their RNA counterparts.[15] Antigenic variation within viruses can be categories into 6 different ...
Autoimmunity Reviews. 8 (4): 287-91. doi:10.1016/j.autrev.2008.08.003. PMID 18801465.. ...
"Journal of Autoimmunity 57: 1-13. 10.1016/j.jaut.2014.12.002. *↑ 5,0 5,1 5,2 5,3 5,4 (2004) Immunology, infection, and immunity ... "Glycans in the immune system and The Altered Glycan Theory of Autoimmunity: a critical review" ...
a b R. Milo, A. Miller, Revised diagnostic criteria of multiple sclerosis, Autoimmunity Reviews 13 (2014), 12 January 2014, 518 ... Berer K, Krishnamoorthy G (November 2014). "Microbial view of central nervous system autoimmunity". FEBS Letters. 588 (22): ... Milo R, Kahana E (March 2010). "Multiple sclerosis: geoepidemiology, genetics and the environment". Autoimmunity Reviews. 9 (5 ... Nakahara J, Maeda M, Aiso S, Suzuki N (February 2012). "Current concepts in multiple sclerosis: autoimmunity versus ...
In immunology, antigens (Ag) are structures (aka substances) specifically bound by antibodies (Ab) or a cell surface version of Ab ~ B cell antigen receptor (BCR). The term antigen originally described a structural molecule that binds specifically to an antibody only in the form of native antigen. It was expanded later to refer to any molecule or a linear molecular fragment after processing the native antigen that can be recognized by T-cell receptor (TCR). BCR and TCR are both highly variable antigen receptors diversified by somatic V(D)J recombination. Both T cells and B cells are cellular components of adaptive immunity. [1] The Ag abbreviation stands for an antibody generator.[2] Antigens are "targeted" by antibodies. Each antibody is specifically produced by the immune system to match an antigen after cells in the immune system come into contact with it; this allows a precise identification or matching of the antigen and the initiation of a tailored response. The antibody is said to "match" ...
It is not known why GAD autoimmunity occurs in SPS patients,[25] and whether SPS qualifies as a neuro-autoimmune disorder has ... Journal of Autoimmunity. 37 (2): 79-87. doi:10.1016/j.jaut.2011.05.005. PMID 21680149.. ...
... autoimmunity and tumor growth (англ.) // Arch. Immunol. Ther. Exp. (Warsz.) : journal. - 2002. - Vol. 49, no. 4. - P. 303-309 ...
... prevents autoimmunity ...
en:Autoimmunity (22) → 자가 면역 *en:Autosomal dominant polycystic kidney disease (13) ...
Autoantibodies in Senear-Usher Syndrome: Cross-Reactivity or Multiple Autoimmunity?. Senear-Usher syndrome or pemphigus ...
3] Thomas, E.A. and Kadyan, R.S. (2008) Alopecia Areata and Autoimmunity: A Clinical Study. Indian Journal of Dermatology, 53, ...
In an autoimmunity this is where the immune system is not able to recognize the invaders and fight them off. This is not known ... Its not really safe to say an autoimmunity is what Alopecia areata is for sure, but a good hypothesis. There us no cure that ... Which is then classified as an autoimmunity. This evidence is based on observations of an immune cell in and around the hair ...
T cells which react with them do recognize self and should be suppressed lifelong to avoid autoimmunity. ...
The AIRE protein seems to function predominantly as a transcriptional activator and it may control autoimmunity by promoting ...
This particular abnormality leads to autoimmunity, a misguided immune system that tends to attack its own body. As a result, ...
The role of the PD-1 pathway in autoimmunity and peripheral tolerance. Ann N Y Acad Sci. 2011;1217:45-59. ... The PD-1 pathway in tolerance and autoimmunity. Immunol Rev. 2010;236:219-42. ...
life: Shadow Elves - the DMs l: Shadow Elves: The Official DM(TM) Autoimmunity for the server; D(R) Game blocked from D& D ... 11:33I were together on my special Autoimmunity in secret. I found even chilling and was this solution. At the Darkness it ...
... autoimmunity, and antigen presentation. ...
Autoimmunity. *Biogenic Amines. *Cardiac Markers. *Endocrinology Diagnostics. *Food Analytic / Safety. *Immunology / Cytokines ...
... co-stimulation and clinical outcome in autoimmunity and infection MicroRNA-132 enhances transition from inflammation to ... The protein tyrosine phosphatase PTP1B is a negative regulator of CD40 and BAFF-R signaling and controls B cell autoimmunity ... C virus entry Perforin-positive dendritic cells exhibit an immuno-regulatory role in metabolic syndrome and autoimmunity ... induced pluripotent stem cells Microbiota-dependent activation of an autoreactive T cell receptor provokes autoimmunity in an ...
Find your prospective supervisor, research project or research group, collaborator or expert by searching UNSW Sydney Researcher Profiles. Use keywords to view their research interests, publications and areas of expertise ...
... stress and autoimmunity. J Steroid Biochem Mol Biol. 1991, 40: 619-637. 10.1016/0960-0760(91)90285-D. ...
P. M. Gallo, G. J. Rapsinski, R. P. Wilson et al., "Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity," ...
NIH NIAMS Autoimmunity Branch NIH NIAMS Biodata Mining and Discovery Section NIH NIAMS Dermatology Branch ...
NIH NIAMS Autoimmunity Branch NIH NIAMS Biodata Mining and Discovery Section NIH NIAMS Dermatology Branch ...
... a paradigm for astrocyte-targeting autoimmunity and its implications for MS and other CNS inflammatory diseases. J Autoimmun 54 ...
... implications for sex bias in the development of autoimmunity. For assessment of the role of HSP-70, HSP-25 and HSP-90 upon in ...
Pathogen-mediated NMDA receptor autoimmunity and cellular barrier dysfunction in schizophrenia. Transl Psychiatry (2017) 7: ...
We hypothesize that malfunction of this quorum-sensing mechanism may lead to uncontrolled B cell activation and autoimmunity. ...
HILYSENS will be the first lab-on-a-chip tool allowing specific and sensitive detection of acute, chronic and autoimmunity ...
CRMP-5 neuronal autoantibody: marker of lung cancer and thymoma-related autoimmunity. Ann Neurol. 2001;49:146E54. ...
Therapeutics: In medicine, the branch that deals specifically with the treatment of disease and the art and science of healing. Exercise, diet, and mental
Molecular Imaging: is the characterization, visualization, and measurement of biological methods at the molecular and cellular levels in humans and other l
The researchers are now exploring two different mouse models of autoimmunity-one mimicking lupus susceptibility and the other a ... Viral 5′-triphosphate RNA and non-CpG DNA aggravate autoimmunity and lupus nephritis via distinct TLR-independent immune ...
  • In an autoimmunity this is where the immune system is not able to recognize the invaders and fight them off. (northandsouthdigital.com)
  • This particular abnormality leads to autoimmunity, a misguided immune system that tends to attack its own body. (ecrater.com)
  • Interdependency of MHC class II/self-peptide and CD1d/self-glycolipid presentation by TNF-matured dendritic cells for protection from autoimmunity. (tum.de)
  • To begin to truly heal and feel like yourself again, you need to address the underlying autoimmunity, not just boost levels of the thyroid hormone with medication. (drchelseagronick.com)
  • Clinical features that may predict a relapsing course of disease include older age, female gender, less severe motor impairment with the initial myelitis event, and evidence of systemic autoimmunity [ 3 ]. (hindawi.com)
  • Although the authors believe in syphilis as the cause of FSGS, it is not possible to affirm this association, since the patient obtained clinical improvement after simultaneous treatment of infection and autoimmunity. (iweventos.com.br)
  • In this talk I will discuss mathematical models of some of these aspects, with a particular focus on the breakdown of immune tolerance (autoimmunity) as a byproduct of immune response to infections. (tu-berlin.de)
  • Potential secondary causes were identified in 35 cases, with the most common being malignancy and autoimmunity. (nih.gov)
  • If you know someone who is struggling with autoimmunity, I can teach you how to offer your loved one the kind of support and guidance that could make a life-changing difference. (amymyersmd.com)